Finkel-Biskis-Reilly mouse osteosarcoma virus v-fos inhibits the cellular response to ionizing radiation in a myristoylation-dependent manner.

The Journal of Biological Chemistry
D W Abbott, J T Holt

Abstract

DNA damage is recognized as a central component of carcinogenesis. DNA-damaging agents activate a number of signal transduction pathways that lead to repair of the DNA, apoptosis, or cell cycle arrest. It is reasoned that a cell deficient in DNA repair is more likely to acquire other cancer-promoting mutations. Despite the recent interest in the link between DNA damage and carcinogenesis, retroviral oncogenes have not yet been shown to affect the DNA damage-signaling pathway. In this report, we show that Finkel-Biskis-Reilly mouse osteosarcoma virus (FBR) v-fos, the retroviral homologue of the c-fos proto-oncogene, inhibits the cellular response to ionizing radiation. Cells that express FBR v-Fos show a decreased ability to repair DNA damage caused by ionizing radiation, and these cells show decreased survival in response to ionizing radiation. In addition, FBR v-Fos inhibits DNA-dependent protein kinase, a kinase specifically activated upon exposure to ionizing radiation. These effects were specific to ionizing radiation, as no effect of FBR v-Fos on the UV light signaling pathway was seen. Last, these effects were dependent on a lipid modification required for FBR v-Fos tumorigenesis, that of myristoylation of FBR v-Fos. A no...Continue Reading

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Citations

Apr 11, 2001·Biochimie·C AcquavivaM Piechaczyk
Jul 17, 1998·Journal of the National Cancer Institute·D W AbbottJ T Holt
Dec 18, 2002·Annals of the New York Academy of Sciences·Claire AcquavivaMarc Piechaczyk
Jul 19, 2006·Progress in Lipid Research·Ponniah SelvakumarRajendra K Sharma
Apr 21, 2001·Oncogene·C AcquavivaI Jariel-Encontre
Sep 17, 2009·Molecular and Cellular Biochemistry·Rong ZhengDavid M Nanus

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